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Diagnostic imaging of the shoulder. Edited By Leanne L. Seeger. Baltimore Williams & Wilkins 1992. 208 PP. Illustrated. Indexed. 90.00

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LETTERS
1030
dial tamponade in patients with systemic lupus erythematosus (SLE). I believe, however, that the discussion of the
pericardial fluid deserves expansion. The pericardial fluids
described in Kahl’s report were characterized as typically
exudative with a “mean number of nucleated cells” of
167/mm3including a mean of 12% neutrophils (range 0-94%).
Although the higher range of neutrophil proportions is noted,
this description gives the impression that pericardial fluids in
SLE are not very dissimilar from other lupoid “effusions”
(pleural, ascitic, joint, and meningeal).
In a 1987 review of pericardial effusions in patients
with idiopathic or drug-induced SLE (2), the mean neutrophi1 percentage in 15 patients was 92% and the mean
reported white blood cell count was almost 30,000/mm3
(although this mean count was influenced by the inclusion of
1 extreme outlier). The fluids were also frequently characterized as bloody. Interestingly, characteristics of the pleural
fluid from 2 patients were different from those of pericardial
fluid obtained simultaneously. As noted by Kahl, there have
been additional reports describing pericardial fluid in SLE
patients (3), which have also demonstrated acute inflammatory features. Hence, I believe that it should be further
emphasized that lupoid pericardial effusions can mimic septic pericarditis, and differ from inflammatory exudates reported from other body sites in SLE.
It would be interesting to know the specific characteristics of the fluid from Kahl’s patient 8 and from any
others in whom abnormalities could conceivably be due to
uremic pericarditis and not to SLE, a difficult distinction to
make clinically in patients with end-stage renal disease
secondary to SLE. Does the frequency of bilateral pleural
effusions or ascites in Kahl’s series differ from that in similar
patients with cardiac tamponade in the absence of SLE?
Brian F. Mandell, MD, PhD
Short Hills, NJ
1. Kahl LE: The spectrum of pericardial tamponade in systemic
lupus erythematosus: report of ten patients. Arthritis Rheum
35~1343-1349, 1992
2. Mandell BF: Cardiovascular involvement in systemic lupus erythematosus. Semin Arthritis Rheum 17:126141, 1987
BOOK REVIEWS
Diagnostic Imaging of the Shoulder. Edited by Leanne L .
Seeger. Baltimore, Williams & Wilkins, 1992. 208 p p . Illustrated. Indexed. $90.00.
Recent books on imaging of regional anatomy have
stressed magnetic resonance imaging (MRI). This compact
volume on shoulder imaging, however, emphasizes a broad
radiologic approach to bone lesions. The editor and authors
have managed to distill the literature and present the imporArthritis and Rheumatism, Vol. 36, No. 7 (July 1993)
3. Zashin SJ, Lipsky PE: Pericardial tamponade complicating systemic lupus erythematosus. J Rheumatol 16:37&377, 1989
Reply
To the Editor:
As Dr. Mandell notes, both in his letter and in his
thorough review of cardiovascular involvement in SLE (l),
pericardial fluid white blood cell and neutrophil counts are
highly variable in lupus pericarditis. Our patient 8, who may
have had pericarditis due to uremia rather than to lupus, did
not have cell counts determined, but his pericardial fluid
protein level of 3.6 mg/dl was indistinguishable from that in
patients with classic SLE pericarditis.
Findings in patient 4, who had samples drawn from
pleural and ascitic as well as pericardial fluids, illustrate Dr.
Mandell’s point about the inflammatory character of pericardial fluids in SLE: The protein level was 4.7 mg/dl in the
pericardial fluid, and 2.6 mg/dl and 2.9 mg/dl in the pleural
fluid and ascitic fluid, respectively. Levels of lactate dehydrogenase in the pericardial, pleural, and ascitic fluids,
respectively, were 442 mg/dl, 243 mg/dl, and 288 mg/dl.
The number of nucleated cells was 19/mm3, 260/mm3, and
99/mm3, and the proportion of neutrophils was 15%, 0%, and
0%, respectively.
Bilateral pleural effusions and/or ascites are notably
rare in patients with cardiac tamponade from causes other
than SLE (2). Fluid collections from these areas in patients
with SLE may be increased in volume due to polyserositis
or, perhaps, to diffuse microvascular permeability (3).
Leslie E. Kahl, MD
Washington University School of Medicine
S t . Louis, MO
Mandell BF: Cardiovascular involvement in systemic lupus erythematosus. Semin Arthritis Rheum l7:126-141, 1987
Guberman BA, Fowler NO, Engel PJ, Gueron M , Allen JM:
Cardiac tamponade in medical patients. Circulation 64:633-640,
1981
Marks J, Birkett DA, Shuster S: “Capillary permeability” in
patients with collagen vascular diseases. Br Med J (Clin Res)
1~782-784, 1972
tant clinical radiologic techniques, with particular emphasis
on the rotator cuff, impingement, instability, and bone
tumors. A diverse collection of authors provides commonsense guidance in the choice of appropriate imaging for
specific clinical problems concerning the shoulder.
The continuing escalation of new technology in radiology has complicated decision-making with regard to specific clinical problems; opposing this trend is the limited
availability of imaging modalities and/or expertise in some
institutions or geographic areas. Then there is the issue of
cost. For example, it is not efficacious, either medically or
economically, to perform an MRI on a shoulder with cuff
BOOK REVIEWS
103 1
arthropathy when plain films will suffice. Furthermore, in the
proper setting, ultrasound to screen for rotator cuff tears
may eliminate the need for either MRI or arthrography. This
book gives enough information to allow the reader to choose
appropriate imaging techniques.
There is enough depth in the excellent chapters on
arthrography, ultrasound, computed arthrotomography, and
MRI to give guidance in decision-making relative to imaging
of specific clinical conditions. While there is some repetition
and even contradiction between authors (indeed, reflecting
the current state of the radiologic imaging field), each
modality is presented by an expert radiologist in his or her
field, with clinical indications, numerous illustrations, and
adequate references. The use of gadolinium (except in a few
specific situations) is not addressed.
Of particular interest are tables comparing published
results of imaging studies with pathologic findings. This is
done for ultrasound of the rotator cuff and for computed
tomographic imaging of the glenoid labrum, but unfortunately not for MRI.
The chapter on bone tumors stresses the use of plain
films with appropriate additional examinations. The 82 illustrations and 131 references make this particular chapter an
excellent primer on the plain film appearance of bone tumors.
There is minimal coverage of arthritis, and the coverage of trauma (other than instability) suffers from excessive text and inadequate graphics, particularly on the classifications of fractures, dislocations, and subluxations. A
minor point: There is incomplete (and perhaps, therefore,
incorrect) discussion of the hypertrophic conditions of the
sternoclavicular joint.
Overall, this is a practical and easily readable addition for general radiologists, rheumatologists, residents,
general orthopedists, physiatrists, physical therapists, and
other practitioners interested in imaging of the shoulder.
Nancy D. Baker, MD
Brigham and Women’s Hospital
Boston, MA
Dubois’ Lupus Erythematosus. Fourth edition. Edited by
Daniel J . Wallace and Bevra Hannahs Hahn. Philadelphia,
Lea & Febiger, 1993. 955 p p . Illustrated. Indexed. $125.00.
Systemic Lupus Erythematosus. Second edition. Edited by
Robert G . Lahita. New York, Churchill Livingstone, 1992.
1,002 pp. Illustrated. Indexed. $1 75.00.
It is certainly a testament to the complexity of
systemic lupus erythematosus that new editions of two
major textbooks have been published in the last year. The
questions to be asked are 1) If I have the previous edition, is
the purchase of the new edition worthwhile; and 2 ) If I plan
to purchase only one, which one?
Both textbooks have undergone major revisions. Of
the two, Dubois’ Lupus Erythematosus has had the most
dramatic changes, with addition of a second editor (Bevra
Hahn), and a new emphasis on the basic immunology
chapters. Both books have included chapters on antiphospholipid antibodies and syndromes. Some chapters in the
two texts are written by the same authors, i.e., those on
epidemiology (Marc Hochberg), antiphospholipid antibodies
(Ronald Asherson), autoantibodies (Morris Reichlin), and
cutaneous lupus (Richard Sontheimer).
There are differences in style and format. Both
textbooks have sections on genetics, epidemiology, immunology, autoantibodies, organ system involvement, and disease management. The chapters on different organ systems
in Systemic Lupus Erythematosus are written by different
authors; in Dubois’ Lupus Erythematosus, Dr. Wallace and
Dr. Francisco Quismorio have written all of the chapters on
organ systems. Dubois’ Lupus Erythematosus textbook is
extensively referenced, including an alphabetized bibliography, author index, and citation index that are extremely
useful in finding that particular “missing” reference.
In a Solomonic manner, I would choose different
areas of special strength in each textbook. Although both
cover antiphospholipid antibodies in detail, the chapters by
E. Nigel Harris (immunology), David Essex and Sandor
Shapiro (lupus anticoagulant), and Asherson (antiphospholipid) are particularly good in Systemic Lupus Erythematosus. Essex and Shapiro, in particular, have written a very
fair and realistic review of lupus anticoagulant assays. There
are a few recommendations in the antiphospholipid antibody
chapters in Dubois’ Lupus Erythematosus that reflect the
confusion and lack of consensus in the field. In the chapter
by Asherson and Richard Cervera, use of the recalcification
test to monitor heparin therapy is recommended (although
recalcification times may be affected by the lupus anticoagulant itself). Prophylactic treatment is recommended for
asymptomatic patients with antiphospholipid antibodies who
are undergoing surgical procedures (at higher-than-usual
doses of heparin, i.e., 25,000 unitslday), and aspirin is
suggested as a prophylactic treatment for asymptomatic
patients with persistently high antiphospholipid levels, without supporting data. In the chapter on lupus anticoagulant by
Donald Feinstein and Robert Francis, aspirin is recommended as the treatment for arterial thrombosis, and the use
of warfarin is labeled as “questionable,” although in their
chapter, Asherson and Cervera do recommend anticoagulation therapy for arterial thrombosis.
The sections on pregnancy and management of lupus
in Dubois’ Lupus Erythemafosus are very good. Rodanthi
Kitridou and Gregorio Mintz have written a chapter on the
mother, one on the fetus, and one on neonatal lupus, all of
which are thorough reviews of controversial areas. (There is
also an excellent review of neonatal lupus by Jill Buyon in
Systemic Lupus Erythematosus.) The seven chapters in
Dubois’ Lupus Erythematousus on disease management,
written (except for the one on corticosteroids) by Dr. Wallace, emphasize nonsteroidal antiinflammatory drug and
antimalarial therapy in addition to the use of cytotoxic
agents. Of course, particular chapters on management in
Systemic Lupus Erythematosus, such as the chapter by John
Klippel, are equally valuable.
In the main, however, the reader will want to “pick
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shoulder, illustrated, 1992, diagnostika, wilkins, seeger, leanne, william, 208, imagine, edited, indexes, baltimore
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