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In vivo LE phenomenon in pleural fluid.

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In Vivo LE Phenomenon in
Pleural Fluid
To the Editor:
In vivo LE cell formation has been documented
in skin ( I ), synovial fluid (2), pericardial fluid (3), and
recently in peritoneal fluid (4). Although the presence of
LE cells in pleural fluid has been mentioned, t o our
knowledge there has been no actual documentation of
this phenomenon.
Case Report. RE, a 49-year-old white female, was
admitted to St. Clare’s Hospital in April 1975 complaining of left pleuritic chest pain, cough, and fever of 4
weeks duration. She developed morning stiffness of the
metacarpophalangeal joints of both hands 2 weeks before admission. There was no history of rash, hair loss,
sunlight sensitivity, or Raynaud’s phenomenon, nor was
there any family history of rheumatic disease. She was
taking no medication.
Examination showed that the patient was not in
acute distress: temperature was 100.8, blood pressure
was 120/80, and the pulse was 90 and regular. The skin
and mucous membranes were normal. There was no
active hair loss or alopecia. Breath sounds at the left
base were dull and decreased. The heart was normal and
the metacarpophalangeal joints of both hands showed
Fig 2. L E prep made from peripheral blood demonstrating typical L E
Fig 1. Chest PA demonstrating left pleural eflusion on admbsion to the
Arthritis and Rheumatism, Vol. 19, No. 5 (September-October 1976)
synovial thickening with moderate tenderness and weakness of the grip bilaterally. There were no nodules. Abdominal and neurologic examinations were normal.
Chest X-ray revealed a left pleural effusion (Figure 1 ).
Laboratory data revealed a hematocrit of 37,
ESR 50 mm/hour, and WBC 4700 with a normal differential. VDRL was negative and ANA was positive 1/20
with a homogeneous pattern. There were three positive
LE preps (Figure 2). Latex fixation was positive 1/20,
C3 complement 85, y-globulin 2.4 mg%, uric acid 1.0
mg%, and sugar 100 mg%. Urinalysis was negative for
protein, sugar, and cells. Intermediate PPD was also
negative. Thoracentesis yielded 200 cm3 of slightly
cloudy yellowish fluid, SG 1.028, with a cell count of
2570/mm3 with 79% lymphocytes, 16% neutrophils, 4%
eosinophils, and 1% monocytes. Protein was 5.0 g%,
LDH 209, and glucose 80 mg%. LE cells were seen on
hematoxylin and eosin stain of the fluid (Figure 3).
1 . Wilson R M , Abbott R R , Miller DK: The occurrence of LE
cells and hematoxylin bodies in naturally occurring cultaneous lesions of SLE. A m J Med Sci 241:31-43, 1961
Hunder GG, Pierre RV: In vivo LE cell formation in synovial fluid. Arthritis Rheum 13:448-451, 1970
Seaman AJ, Christerson JW: Demonstration of LE cells in
pericardial fluid. JAMA 149:145-147, 1951
Metzger AL, Coyne M, Lee S, et al: In vivo LE cell formation in peritonitis due to SLE. J Rheumatol 1:130-133, 1974
Dubois EL: Lupus Erythematosus. Second edition. Los
Angeles, University of California Press, 1974, pp 528-531
Dubois EL: Lupus Erythematosus. Second edition. Los
Angeles, University of California Press, 1974, p 254
Resident in Internal Medicine
Chief, Rheumatology Division
Chairman, Department of Medicine
St. Clare’s Hospital
415 West 51st Street
New York, New York 10019
Antibodies to DNA :
False Positive Results?
To the Editor:
Fig 3. Hematoxylin and eosin stain of pleuraljluid demonstrating LE
Cultures of the fluid were negative for bacteria.
Treatment with 20 mg of prednisone resulted in
rapid defervescence of fever and resolution of joint findings and pleural effusion over 4 weeks.
Discussion. The patient presented with three major criteria (pleuritis, synovitis, and LE cells) and two
minor criteria (fever and hypergammaglobulinemia)
and thus was diagnosed as a case of systemic lupus
erythematosus (SLE) (5). Pleuritis and pleural effusions
are rare initial manifestations of SLE. Dubois recorded
the onset of SLE with pleurisy and effusion in only 3.9%
and I .9% of 520 cases respectively (6). Nevertheless the
presence of LE cells, a normal pleural fluid sugar, and
an exudative pleural fluid is more consistent with SLE
than with rheumatoid arthritis or infection. It can therefore be seen once again that LE cells may appear in vivo
in various effusions of SLE and may be helpful in the
early diagnosis of this disease.
We believe that the positive tests for antibodies to
double-stranded DNA (dsDNA) in 18 patients with RA
and 5 patients with JRA reported by Bell, Tala], and
Schur (A&R 18535-540, 1975) may be false positive
results produced by testing with unpurified mammalian
dsDNA preparations. These in all probability contain
single-stranded DNA (ssDNA) and/or dsDNA with ss
regions. Therefore we believe that their conclusion that
anti-dsDNA-antibodies can be found in these diseases
may not be justified.
We have found that commercial mammalian
dsDNA (14C KB cell DNA) can be fractionated on benzoylated naphthoylated DEAE cellulose (BNDC). Using this technique, we have found that only 25% of the
DNA in this preparation is native dsDNA. the bulk of
the remainder being dsDNA with ss regions ( I ) . This
major contaminant is not detectable on hydroxyapatite.
We have employed “C native dsDNA purified in this
way, as well as chromatographically purified 3H dsDNA
and ssDNA prepared from T7 and @XI74 bacteriophages, respectively, to determine the specificities of
anti-DNA antibodies in 10 non-SLE sera previously
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pleural, phenomena, vivo, fluid
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